Fig. 1.

Average developed (systolic-diastolic) left ventricular pressure (LVP) 120 min after global IR injury when isolated guinea pig hearts were perfused without ischemia (Time Controls, TC); with 35 min ischemia and 120 min reperfusion (IR); or with IR + BK_Ca and or SK_Ca channel agonists (A); IR + BK_Ca and or SK_Ca channel antagonists (B); IR + BK_Ca agonist and or BK_Ca, SK_Ca antagonists (C); IR + BK_Ca agonist and or SK_Ca or BK_Ca antagonist (D); and SOD dismutator + BK_Ca and or SK_Ca agonist (E). Developed LVP over time for the IR only, IR + SK_Ca agonist and SK_Ca + BK_Ca agonist groups are displayed (F). Note the worsened effects on developed LVP of BK_Ca and BK_Ca + SK_Ca antagonists (green bars) vs. IR only (red bars); the block of protection by the BK_Ca or SK_Ca agonists when the BK_Ca or SK_Ca antagonists, respectively, was present (green bars); the maintained protection by the BK_Ca and or SK_Ca agonists in the presence of either the SK_Ca or the BK_Ca antagonist, respectively, (blue bars); and the loss of protection by the SK_Ca and or BK_Ca agonists in the presence of SOD inhibition by TBAP (orange/green bars). For each treatment group n = 5–6 hearts; note that for 32 of these hearts’ mitochondria were isolated after 20 min reperfusion to assess RCI and CRC (Figs. 4,5). Data expressed as mean ± sem. *^,§ P<0.05.